Crown gall induced by Agrobacterium vitis is a worldwide plant disease in grape-growing regions. Rahnella aquatilis HX2, a new isolate from vineyard soil in Beijing, showed a significant inhibition effect on the development of crown galls in grapevines. In field trials, immersion of the basal ends of grape cuttings with HX2 cell suspension inhibited or completely prevented crown gall formation caused by A. vitis K308 in the roots of the plants from the cuttings. The 3-year average disease incidence in grape plants treated with HX2 was 30.8% compared to 93.5% in plants without HX2. The culture supernatant of HX2 exhibited a stronger inhibition effect on disease development than did the cell suspension. HX2 could be found in the grape rhizosphere, grown under field conditions, for up to 90 days after inoculation. There was no significant difference in the mean population sizes of root microflora between plants treated and not treated with HX2. The inhibition effect of HX2 on crown gall in sunflower, caused by different agrobacterial strains, varied between 30.7 and 100%, depending on strains. Our results showed that Rahnella aquatilis HX2 may be used as a biological control agent for crown gall disease of grapes.

Piglets obtaining milk from anterior and middle mammary glands (MG) grow faster than those suckling posterior MG, but the underlying mechanisms are not clear. The purpose of this study was to investigate the differential proteomes of colostrum and milk secreted by anterior and posterior MG. Six healthy primiparous sows with 7 pairs of MG were used; the first and the second pairs were defined as anterior MG and the sixth and seventh pairs as posterior MG. Colostrum and milk were collected at d 1 and 14 after parturition, respectively. Comparative proteomics analysis was performed to identify the differentially expressed proteins in colostrum and milk secreted by anterior and posterior MG. Results show that protein composition in colostrum and milk varied markedly with the anatomical location of MG. Immunoglobulins, lactadherin, and haptoglobin were upregulated (P < 0.05) in colostrum from anterior MG compared with posterior MG. Concentrations of immunoglobulins and lactoferrin in milk from anterior MG were greater (P < 0.05) than milk from posterior MG. Moreover, concentration of proteins from somatic cells was greater (P < 0.05) in milk from posterior MG compared with anterior MG. Most proteins, in which abundance was upregulated in colostrum and milk from anterior MG, contribute to passive immunity, intestinal development of suckling piglets and epithelial integrity, and the health of MG. Collectively, these results indicate that in comparison with posterior MG, anterior MG are more active in protein synthesis and produce more immunoglobulins and lactoferrin in colostrum and milk.

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In 2012, significant brown rot disease was observed on stone fruit in Pennsylvania, Maryland, and South Carolina despite preharvest application of methyl benzimidazole carbamate (MBC) and demethylase inhibitor (DMI) fungicides. In total, 140 Monilinia fructicola isolates were collected from diseased orchards and examined for fungicide sensitivity. In addition to isolates resistant to either the DMI propiconazole or the MBC thiophanate-methyl, 22 isolates were discovered that were resistant to both fungicides, including 4 isolates from peach in South Carolina, 12 isolates from peach and sweet cherry in Maryland, and 6 isolates from sweet cherry in Pennsylvania. Analysis of MBC resistance revealed that dual-resistant isolates from South Carolina carried the β-tubulin E198A mutation, whereas isolates from Maryland and Pennsylvania carried E198 mutations not previously described in the Monilinia genus, E198Q or F200Y. The genetic element Mona, associated with DMI fungicide resistance in M. fructicola, was detected in the dual-resistant isolates from South Carolina but not in the isolates from the two more northern states. An investigation into the molecular mechanism of DMI resistance in the latter isolates revealed that resistance was not based on increased expression or mutation of MfCYP51, which encodes the target of DMI fungicides. Label rates of formulated propiconazole or thiophanate-methyl were unable to control dual-resistant isolates on detached peach fruit, confirming field relevance of dual resistance. The same isolates were not affected by fitness penalties based on mycelial growth rate, ability to sporulate, and virulence on detached peach fruit. The emergence of M. fructicola strains resistant to both DMI and MBC fungicides in multiple states and multiple stone fruit crops is a significant development and needs to be considered when designing resistance management strategies in stone fruit orchards.

Fusarium verticillioides reduces corn yield and contaminates infected kernels with the toxin fumonisin, which is harmful to humans and animals. Previous research has demonstrated that F. verticillioides can be controlled by the azole fungicide prochloraz. Currently, prochloraz is used as a foliar spray to control maize disease in China, which will increase the risk of resistance. Although F. verticillioides resistance to prochloraz has not been reported in the field, possible resistance risk and mechanisms resulting in prochloraz resistance were explored in the laboratory. Four prochloraz-resistant strains of F. verticillioides were generated by successive selection on fungicide-amended media. The mycelial growth rates of the mutants were inversely related to the level of resistance. All four mutants were cross-resistant to the triazole fungicides triadimefon, tebuconazole and difenoconazole, but not to the multisite fungicide chlorothalonil or to the MAP/histidine-kinase inhibitor fungicide fludioxonil. Based on the Y123H mutation in FvCYP51B, the four resistant mutants were subdivided into two genotypes: PCZ-R1 mutants with wildtype FvCYP51B and PCZ-R2 mutants with substitution Y123H in FvCYP51B. Wildtype FvCYP51B complemented the function of native ScCYP51 in Saccharomyces cerevisiae YUG37::erg11, whereas Y123H-mutated FvCYP51B did not. For the PCZ-R1 mutants, induced expression of FvCYP51A increased resistance to prochloraz. For the PCZ-R2 mutants, disruption of FvCYP51B function by the Y123H substitution caused constitutive up-regulation of FvCYP51A expression and thus resistance to prochloraz.